50–90% female adolescents and women of reproductive age[4]
Dysmenorrhea, also known asperiod pain,painful periods ormenstrual cramps, ispain duringmenstruation.[4][5][2] Its usual onset occurs around the time that menstruation begins.[1] Symptoms typically last less than three days.[1] The pain is usually in thepelvis or lower abdomen.[1] Other symptoms may includeback pain, diarrhea or nausea.[1]
Estimates of the percentage of femaleadolescents and women of reproductive age affected are between 50% and 90%.[4][6] It is the most commonmenstrual disorder.[2] Typically, it starts within a year of thefirst menstrual period.[1] When there is no underlying cause, often the pain improves with age or following having a child.[2]
The main symptom of dysmenorrhea is pain concentrated in the lowerabdomen orpelvis.[1] It is also commonly felt in the right or left side of the abdomen. It may radiate to thethighs and lowerback.[1]
Symptoms often co-occurring with menstrual pain includenausea andvomiting,diarrhea,headache,dizziness,disorientation,fainting andfatigue.[7] Symptoms of dysmenorrhea often begin immediately after ovulation and can last until the end of menstruation. This is because dysmenorrhea is often associated with changes in hormonal levels in the body that occur with ovulation. In particular,prostaglandins induce abdominal contractions that can cause pain and gastrointestinal symptoms.[8][9] The use of certain types of birth control pills can prevent the symptoms of dysmenorrhea because they stop ovulation from occurring.
For many, primary dysmenorrhea symptoms gradually subside after their mid-20s. Pregnancy has also been demonstrated to lessen the severity of dysmenorrhea, when menstruation resumes. However, dysmenorrhea can continue untilmenopause. 5–15% of women with dysmenorrhea experience symptoms severe enough to interfere with daily activities.[12]
There are two types of dysmenorrhea, primary and secondary, based on the absence or presence of an underlying cause. Primary dysmenorrhea occurs without an associated underlying condition, while secondary dysmenorrhea has a specific underlying cause, typically a condition that affects the uterus or other reproductive organs.[5]
Painful menstrual cramps can result from an excess ofprostaglandins released from the uterus. Prostaglandins cause the uterine muscles totighten and relax causing the menstrual cramps. This type of dysmenorrhea is calledprimary dysmenorrhea.[5] Primary dysmenorrhea usually begins in the teens soon after thefirst period.[13]
Membranous dysmenorrhea is a type of secondary dysmenorrhea in which the entire lining of the uterus is shed all at once rather than over the course of several days as is typical.[15] Signs and symptoms include spotting, bleeding, abdominal pain, and menstrual cramps. The resulting uterine tissue is called a decidual cast and must be passed through the cervix and vagina.[16] It typically takes the shape of the uterus itself. Membranous dysmenorrhea is extremely rare and there are very few reported cases. The underlying cause is unknown, though some evidence suggests it may be associated with ectopic pregnancy or the use of hormonal contraception.
Whenlaparoscopy is used for diagnosis, the most common cause of dysmenorrhea is endometriosis, in approximately 70% of adolescents.[17]
Genetic factors, stress and depression are risk factors for dysmenorrhea.[22] Risk factors for primary dysmenorrhea include: early age atmenarche, long or heavy menstrual periods, smoking, and a family history of dysmenorrhea.[12]
Dysmenorrhea is a highlypolygenic andheritable condition.[23] There is strong evidence of familial predisposition and genetic factors increasing susceptibility to dysmenorrhea. There have been multiplepolymorphisms and genetic variants in both metabolicgenes and genes responsible forimmunity which have been associated with the disorder.[24]
Three distinct possiblephenotypes have been identified for dysmenorrhea which include "multiple severe symptoms", "mild localized pain", and "severe localized pain". While there are likely differences ingenotypes underlying each phenotype, the specific correlating genotypes have not yet been identified. These phenotypes are prevalent at different levels in different population demographics, suggesting different allelic frequencies across populations (in terms of race, ethnicity, and nationality).[25]
Polymorphisms in theESR1 gene have been commonly associated with severe dysmenorrhea.[23] Variant genotypes in the metabolic genes such asCYP2D6 andGSTM1 have been similarly been correlated with an increased risk of severe menstrual pain, but not with moderate or occasional phenotypes.[26]
The occurrence and frequency of secondary dysmenorrhea (SD) has been associated with differentalleles and genotypes of those with underlyingpathologies, which can affect thepelvic region or other areas of the body. Individuals with disorders may have geneticmutations related to their diagnoses which produce dysmenorrhea as a symptom of their primary diagnosis. It has been found that those withfibromyalgia who have the ESR1 gene variation Xbal and possess the Xbal AA genotype are more susceptible to experiencing mild to severe menstrual pain resulting from their primary pathology.[27] Commonly, genetic mutations which are a hallmark of or associated with specific disorders can produce dysmenorrhea as a symptom which accompanies the primary disorder.
In contrast with secondary dysmenorrhea, primary dysmenorrhea (PD) has no underlying pathology.[28] Genetic mutation and variations have therefore been thought to underlie this disorder and contribute to the pathogenesis of PD.[29] There are multiplesingle-nucleotide polymorphisms (SNP) associated with PD. Two of the most well studied include an SNP in thepromoter ofMIF and an SNP in thetumor necrosis factor (TNF-α) gene. When acytosine 173 base pairs upstream ofmacrophage migration inhibitory factor (MIF) promoter was replaced by aguanine there was an associated increase in the likelihood of the individual experiencing PD. While a CC/GG genotype led to an increase in likelihood of the individual experiencing severe menstrual pain, a CC/GC genotype led to a more significant likelihood of the disorder impacting the individual overall and increasing the likelihood of any of the three phenotypes.[30] A second associated SNP was located 308 base pairs upstream from the start codon of the TNF-α gene, in which guanine was substituted foradenine. A GG genotype at the loci is associated with the disorder and has been proposed as a possible genetic marker to predict PD.[30]
There has also been an association with mutations in theMEFV gene and dysmenorrhea, which are considered to be causative.[31] The phenotypes associated with these mutations in the MEFV genes have been better studied; individuals who areheterozygous for these mutations are more likely to be affected by PD which presents as a severe pain phenotype.[23]
Genes related to immunity have been identified as playing a significant role in PD as well.IL1A was found to be the gene most associated with primary dysmenorrhea in terms of its phenotypic impact.[23] This gene encodes a protein essential for the regulation of immunity and inflammation. While the mechanism of how it influences PD has yet to be discovered, it is assumed that possible mutations in IL1A or genes which interact with it impact the regulation of inflammation during menstruation. These mutations may therefore affect pain responses during menstruation which lead to the differing phenotypes associated with dysmenorrhea.
Two additionally well-studied SNPs which are suspected to contribute to PD were found in ZM1Z1 (the mutant allele called rs76518691) and NGF (the mutant allele called rs7523831). BothZMIZ1 andNGF are associated withautoimmune responses anddiseases, as well as pain response.[23] The implication of these genes impacting dysmenorrhea is significant as it suggests mutations which affect the immune system (specifically the inflammatory response) and pain response may also be a cause of primary dysmenorrhea.
During an individual's menstrual cycle, theendometrium thickens in preparation for potentialpregnancy. Afterovulation, if theovum is notfertilized and there is no pregnancy, the built-up uterine tissue is not needed and thus shed.
Prostaglandins andleukotrienes are released during menstruation, due to the build up ofomega-6 fatty acids.[33][34] Release of prostaglandins and other inflammatory mediators in theuterus cause the uterus to contract and can result in systemic symptoms such as nausea, vomiting, bloating and headaches or migraines.[33] Prostaglandins are thought to be a major factor in primary dysmenorrhea.[35] When the uterine muscles contract, theyconstrict the blood supply to the tissue of the endometrium, which, in turn, breaks down and dies. These uterine contractions continue as they squeeze the old, dead endometrial tissue through thecervix and out of the body through thevagina. These contractions, and the resulting temporary oxygen deprivation to nearby tissues, are thought to be responsible for the pain or cramps experienced during menstruation.
Compared with non-dysmenorrheic individuals, those with primary dysmenorrhea have increased activity of the uterine muscle with increased contractility and increased frequency of contractions.[36]
The diagnosis of dysmenorrhea is usually made simply on amedical history of menstrual pain that interferes with daily activities. However, there is no universally accepted standard technique for quantifying the severity of menstrual pains.[37] There are various quantification models, called menstrual symptometrics, that can be used to estimate the severity of menstrual pains as well as correlate them with pain in other parts of the body,menstrual bleeding and degree of interference with daily activities.[37]
Once a diagnosis of dysmenorrhea is made, further workup is required to search for any secondary underlying cause of it, in order to be able to treat it specifically and to avoid the aggravation of a perhaps serious underlying cause.
Further work-up includes a specificmedical history of symptoms and menstrual cycles and apelvic examination.[6] Based on results from these, additional exams and tests may be motivated, such as:
Treatments that target the mechanism of pain includenon-steroidal anti-inflammatory drugs (NSAIDs) and hormonal contraceptives. NSAIDs inhibit prostaglandin production. With long-term treatment, hormonal birth control reduces the amount of uterine fluid/tissue expelled from the uterus. Thus resulting in shorter, less painful menstruation.[38] These drugs are typically more effective than treatments that do not target the source of the pain (e.g. acetaminophen).[39] Regular physical activity may limit the severity of uterine cramps.[12][40]
Use ofhormonal birth control may improve symptoms of primary dysmenorrhea.[42][33] A 2009 systematic review (updated in 2023) found evidence that the low or medium doses of estrogen contained in the birth control pill reduces pain associated with dysmenorrhea.[43] In addition, no differences between different birth control pill preparations were found.[43] The review did not determine if the estrogen in birth control pills was more effective than NSAIDs.[43]
A review indicated the effectiveness oftransdermalnitroglycerin.[48]Reviews indicatedmagnesium supplementation seemed to be effective.[49][2]A review indicated the usefulness of usingcalcium channel blockers.[32]Heat is effective compared to NSAIDs and is a preferred option by many patients, as it is easy to access and has no known side effects.[50]
Tamoxifen has been used effectively to reduce uterine contractility and pain in dysmenorrhea patients.[51]
There is some evidence that exercise performed three times a week for about 45 to 60 minutes, without particular intensity, reduces menstrual pain.[40]
One review foundthiamine and vitamin E to be likely effective.[54] It found the effects of fish oil andvitamin B12 to be unknown.[54] Reviews found tentative evidence thatginger powder may be effective for primary dysmenorrhea.[55] Reviews have found promising evidence forChinese herbal medicine for primary dysmenorrhea, but that the evidence was limited by its poor methodological quality.[56][57]
A 2016Cochrane review ofacupuncture for dysmenorrhea concluded that it is unknown if acupuncture oracupressure is effective.[58] There were also concerns ofbias in study design and in publication, insufficient reporting (few looked atadverse effects), and that they were inconsistent.[58] There are conflicting reports in the literature, including one review which found that acupressure, topical heat, and behavioral interventions are likely effective.[54] It found the effect of acupuncture andmagnets to be unknown.[54]
A 2007 systematic review found some scientific evidence that behavioral interventions may be effective, but that the results should be viewed with caution due to poor quality of the data.[59]
Spinal manipulation does not appear to be helpful.[54] Although claims have been made forchiropractic care, under the theory that treatingsubluxations in thespine may decrease symptoms,[60] a 2006 systematic review found that overall no evidence suggests thatspinal manipulation is effective for treatment of primary and secondary dysmenorrhea.[61]
Dysmenorrhea is one of the most common gynecological problems, regardless of age or race. It is one of the most frequently identified causes of pelvic pain in those who menstruate. Dysmenorrhea is estimated to affect between 50% and 90% of female adolescents and women of reproductive age.[4] Another report states that estimates can vary between 16% and 91% of surveyed individuals, with severe pain observed in 2% to 29% of menstruating individuals.[50] Reports of dysmenorrhea are greatest among individuals in their late teens and 20s, with reports usually declining with age. The prevalence inadolescent females has been reported to be 67.2% by one study[63] and 90% by another.[64] It has been stated that there is no significant difference in prevalence or incidence between races,[64] although one study ofHispanic adolescent females indicated an elevated prevalence and impact in this group.[65] Another study indicated that dysmenorrhea was present in 36.4% of participants, and was significantly associated with lower age and lowerparity.[66]Childbearing is said to relieve dysmenorrhea, but this does not always occur. One study indicated that innulliparous individuals with primary dysmenorrhea, the severity of menstrual pain decreased significantly after age 40.[67]
A survey inNorway showed that 14 percent of females between the ages of 20 and 35 experience symptoms so severe that they stay home from school or work.[68] Among adolescent girls, dysmenorrhea is the leading cause of recurrent short-term school absence.[69]
A study fromIndia conducted by Dr RimJhim Kumari found that painful menstruation affected 66.7% of adolescent girls studied, of which 27% sought medical advice from a doctor.[70]
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